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A Comparison of Cytokine Profiles of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis and Multip

Discussion in 'Latest ME/CFS Research' started by JaimeS, Nov 12, 2015.

  1. JaimeS

    JaimeS Senior Member

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    A Comparison of Cytokine Profiles of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis Patients

    Author(s) Leave a comment
    Naomi Wong1, Thao Nguyen1, Ekua Weba Brenu1, Simon Broadley2,3, Donald Staines1,2, Sonya Marshall-Gradisnik1,2

    Affiliation(s):

    1National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Centre, School of Medical Science, Griffith University, Gold Coast, Australia.
    2School of Medicine, Gold Coast Campus, Griffith University, Gold Coast, Australia.
    3Department of Neurology, Gold Coast University Hospital, Gold Coast, Australia.

    ABSTRACT:

    Background: Chronic Fatigue Syndrome, also known as Myalgic Encephalomyelitis (CFS/ME), is a debilitating condition that presents with a range of symptoms, including fatigue, cognitive dysfunction, muscular and joint pain, and may be immune-mediated. In particular, patients exhibit abnormal cytokine expression. Similarly, in Multiple Sclerosis (MS), patients display neuroimmunological symptoms, and abnormal cytokine expression, with some overlap in symptomology with CFS/ME.

    The purpose of this study was to compare Th1, Th2, Th17 cytokines, inflammatory cytokines and chemokines, in healthy controls, CFS/ME and MS patients.

    Methods:

    Serum samples were collected from healthy controls (n = 16, mean age = 50 ± 11.85 years), CFS/ME patients (n = 16, mean age = 49.88 ± 9.54 years) and MS patients (n = 11, mean age = 52.75 ± 12.81 years). The concentrations of 27 cytokines (IFN-γ, TNF-α, IL-12, IL-2, IL-1β, IL-4, IL-6, IL-10, IL-13, IL-5, IL-17, IL-1ra, IL-7, IL-8, IL-9, eotaxin, IP-10, MCP-1, MIP1α, MIP1β, PDGF-bb, RANTES, basic FGF, GCSF, GMCSF, VEGF and IL-15) were measured using a Bio-Plex Pro™ kit.

    Results:

    IFN-γ, IL-10 and IL-5 were significantly higher in the serum of both CFS/ME and MS patients compared to the healthy controls (p ≤ 0.041). However, only the MS patients had significantly elevated levels of IL-12, IL-1β, IL-4, IL-13, IL-6, IL-17, IL-1ra, IL-7, IL-9, eotaxin, IL-10, MIP1α, basic FGF, GCSF and VEGF compared to the CFS/ME patients and controls (p ≤ 0.04).

    There were no significant differences between groups for IL-8, MCP-1, MIP1β, RANTES, GMCSF, TNF-α, and IL-2.

    Conclusion:

    CFS/ME and MS patients both displayed abnormal cytokine levels, with dual expression of Th1 and Th2 cytokines. Further research into cytokines such as IFN-γ, IL-10 and IL-5, with the use of a specific CFS/ME case definition and sensitive cytokine assays, is required to improve the understanding of the pathophysiology of CFS/ME.

    KEYWORDS

    Chronic Fatigue Syndrome, Multiple Sclerosis, Immunology, Cytokine

    Cite this paper:

    Wong, N. , Nguyen, T. , Brenu, E. , Broadley, S. , Staines, D. and Marshall-Gradisnik, S. (2015) A Comparison of Cytokine Profiles of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis Patients. International Journal of Clinical Medicine, 6, 769-783. doi: 10.4236/ijcm.2015.610103.



    Some of the spacing is mine, and the boldface is mine. I wanted to make it a wee bit easier for those of us with some focus issues to read and get the nuggets from it. :)

    Appears to be a follow-up to the Hornig, but the number of patients in each group is pretty darned small... and they did NOT separate the groups into newer or older patient groups. In fact, it's pretty disappointing, because it does not appear on first glance that they addressed this at all; these patients could have been predominantly ill longer, or maybe shorter, or maybe it's an even mix... no way to tell. The fact that some cytokines are persistently elevated seems potentially interesting, but again, it's hard to say because it doesn't appear they took time into account.

    Full text is available at the link.

    -J
     
    Last edited: Nov 12, 2015
    J.G, justy, jimells and 6 others like this.
  2. msf

    msf Senior Member

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    I hate to be negative about biomedical research into ME, but I think studies like this that use the Fukuda criteria are a waste of time and money, and can actually obfuscate matters.
     
    medfeb likes this.
  3. Sidereal

    Sidereal Senior Member

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    I think we should be as critical of poor-quality medical research as we are of biopsychosocial research.
     
    Solstice, jimells, halcyon and 5 others like this.
  4. SOC

    SOC

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    I wouldn't call this poor quality research. I'd prefer researchers used a tighter defintion than Fukuda at this time, but unfortunately, Fukuda is the currently accepted research definition internationally. As long as they are clear about the limitations of their research -- and all research has limitations -- and haven't spun the results, this can be useful information. I don't expect it to be definitive, and I doubt they do either, based on their conclusion. It's a contribution to the biomedical information database, which we need.
     
    JaimeS and A.B. like this.
  5. adreno

    adreno PR activist

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    They don't seem to have learned from Lipkin et al., regarding short vs long term ME.
     
    Solstice, Sidereal, Mij and 2 others like this.
  6. JaimeS

    JaimeS Senior Member

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    The quality of the article is disappointing. They should at least be aware of one of the most well-known studies on ME to date! (Hornig et al.) Additionally, the multiple spelling and grammar errors make it look like it was typed up over the weekend.

    It's not always true that better money nets better quality, but it is difficult to attract a wide variety of high-quality research on the strength of goodwill alone. Yes, there are those who will fight the good fight for funding, but they are few and far between. Honestly, I'm happy that, with the situation as it is, our condition has managed to attract some scientific minds of quality.

    Still, I do think it's good to be aware of poor research as well as good research, if only to be able to point out flaws to those who would cite/use the data.

    -J
     
    jimells, SOC, Simon and 1 other person like this.
  7. Sidereal

    Sidereal Senior Member

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    Well, an N=16 study examining 27 cytokines is poor quality research. They have more outcomes than patients. The study is grossly underpowered to do what it wants to do and the results are likely to be due to chance. So, it's not a contribution to the biomedical information database, it just pollutes the database with statistical nonsense. I am sorry if that upsets anyone here or any researchers who might be reading Phoenix Rising. We already know from the Hornig/Lipkin data that one important way in which an ME/CFS cohort must be stratified is by illness duration. This group is continuing to ignore this very important information and keeps putting out papers where patients are not stratified or stratified only based on symptom severity or depending on which criteria they meet, neither of which have been shown in a large dataset to be a meaningful predictor of cytokine levels in ME/CFS.
     
    Jill, J.G, Solstice and 5 others like this.
  8. JaimeS

    JaimeS Senior Member

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    Here is research done by this group. (Sorry, wrong link! I fixed it.) It is surprising how so much of it is VERY modern but doesn't take the excitation-exhaustion implications of Hornig's study into account. It is like they set out in a certain direction and have continued stomping forward regardless of what newer research implies.

    Would you guys rather just not see poorer-quality studies? Reading them does help inform me, even if it is an exercise in what not to do. (For example, I read the number of participants and thought, "that's not significant..." but @Sidereal 's observation that there were "more outcomes than patients" was valuable to me.)


    -J
     
  9. adreno

    adreno PR activist

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    I think it's good they are posted on the forum.
     
  10. jimells

    jimells Senior Member

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    Please keep posting and analyzing these studies. I have no background in research or evaluating it, but I definitely want to learn how to analyze the research, since I am unable to find knowledgeable doctors (although some are open to learning about my illness).
     
    Solstice, mango, Valentijn and 2 others like this.
  11. halcyon

    halcyon Senior Member

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    This study was done on an ICC ME cohort, not Fukuda. This may be one explanation of why it differs from Hornig et al. as they used Fukuda/CCC.
     
  12. msf

    msf Senior Member

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    Yes, I think I overreacted somewhat anyway.
     

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